OBJECTIVE: To evaluate changes in quinolinic acid production in response to viral infection and disease progression. RESULTS Previously we demonstrated that the neurotoxin, quinolinic acid, is increased in both systemic circulation and the intrathecal compartment following retroviral infection. We have now begun to investigate the potential sources of QUIN within the CNS. QUIN within the CNS may derive from diffusion across the blood-brain-barrier or may reflect endogenous production with the CNS by cells related to the monocyte/macrophage lineage. Previously collected, frozen postmortem tissue samples from infected animals are being analyzed to determine the regional distribution of QUIN within the brain. FUTURE DIRECTIONS One future direction would be to test the effectiveness of NMDA receptor antagonists in blocking the adverse effects of QUIN on neural tissue. KEY WORDS quinolinic acid, blood-brain-barrier, simian immunodeficiency virus, cerebrospinal fluid NIMH MH41659